ArticleJournal of orthopaedic surgery and research2026
The role and mechanism of miR-875-3p in targeting SLC39A14 to regulate ferroptosis in osteosarcoma proliferation, migration, and invasion.
Article in Journal of orthopaedic surgery and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundOsteosarcoma is a common primary bone malignancy with poor prognosis. While microRNA dysregulation has been implicated in osteosarcoma progression, the role of exosome-mediated miRNAs, particularly miR-875-3p, in regulating ferroptosis and tumor progression remains unclear. This study aimed to investigate whether miR-875-3p promotes osteosarcoma proliferation, migration, and invasion by targeting SLC39A14 and inhibiting ferroptosis.
methodsExosomes were isolated from osteosarcoma tissues and H143B cells, then characterized by transmission electron microscopy as well as Western blot. Bioinformatics analysis and dual-luciferase assays identified SLC39A14 as a direct target of miR-875-3p. Lentiviral and adenoviral transfection were used to knockdown miR-875-3p and SLC39A14 in H143B cells. Cell viability, migration, and invasion were assessed using CCK-8, wound healing, and Transwell assays. Ferroptosis markers (GSH/GSSG, Fe²⁺, ROS, MDA) and related genes (GPX4, ACSL4, xCT) were eventually measured.
resultsExosomes isolated from osteosarcoma tissues exhibited a typical spherical morphology and were positive for exosomal markers (HSP70, TSG101). MiR-875-3p was upregulated in osteosarcoma tissues and cell-derived exosomes, while SLC39A14 was downregulated. Knockdown of miR-875-3p upregulated SLC39A14, promoted ferroptosis, and suppressed osteosarcoma cell proliferation, migration, and invasion in vitro. In contrast, SLC39A14 knockdown attenuated ferroptosis and enhanced malignant phenotypes. In vivo, miR-875-3p knockdown inhibited tumor growth, whereas SLC39A14 knockdown promoted it.
conclusionmiR-875-3p promotes osteosarcoma progression by targeting SLC39A14 and suppressing ferroptosis, suggesting the miR-875-3p/SLC39A14 axis as a potential therapeutic target for osteosarcoma treatment.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.